| + |
PTGS1 | up-regulates quantity 
chemical modification
|
prostaglandin G2(1-) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269771 |
|
|
in vitro |
|
| pmid |
sentence |
| 7592599 |
[14C]Arachidonate metabolism by oPGHS-1 and hPGHS-2 was examined in reactions with a series of GSP/Cox ratios (Fig. 3). The principal metabolite for both isoforms was the endoperoxide PGH2, with lesser amounts of PGF2a, PGE2, PGD2, |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
naproxen | down-regulates activity 
chemical inhibition
|
PTGS1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258603 |
|
|
in vitro |
|
| pmid |
sentence |
| 9057869 |
Naproxen had similar activity against both COX-1 and COX-2 enzymes (IC50s of 3.2 and 2.5 μM, respectively), whereas ibuprofen was approximately 100-fold more potent for COX-2 (IC50 = 0.1 μM) than for COX-1 (IC50 = 11 μM), and indomethacin was about 50-fold more potent for COX-1 (IC50 = 0.012 μM) than for COX-2 (IC50 = 0.56 μM). |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
ketoprofen | down-regulates activity
chemical inhibition
|
PTGS1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257810 |
|
|
Homo sapiens |
PC-3 Cell |
| pmid |
sentence |
| 18667313 |
Profens, that is, Ketoprofen 1, Suprofen 2 (Fig. 1), were chosen because of their interesting inhibitory activity against cyclooxygenase and of their different selectivity versus the two isoforms COX-1/COX-2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
indometacin | down-regulates activity
chemical inhibition
|
PTGS1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258607 |
|
|
in vitro |
|
| pmid |
sentence |
| 9057869 |
Naproxen had similar activity against both COX-1 and COX-2 enzymes (IC50s of 3.2 and 2.5 μM, respectively), whereas ibuprofen was approximately 100-fold more potent for COX-2 (IC50 = 0.1 μM) than for COX-1 (IC50 = 11 μM), and indomethacin was about 50-fold more potent for COX-1 (IC50 = 0.012 μM) than for COX-2 (IC50 = 0.56 μM). |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
ibuprofen | down-regulates activity
chemical inhibition
|
PTGS1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258883 |
|
|
in vitro |
|
| pmid |
sentence |
| 9544212 |
The IC50 values for two benchmark compounds were determined for comparison. The marketed NSAID ibuprofen was a modestly selective COX-1 inhibitor, while Searle's SC-5766614 was a highly selective (>100-fold) COX-2 inhibitor, results consistent with literature reports. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258605 |
|
|
in vitro |
|
| pmid |
sentence |
| 9057869 |
Naproxen had similar activity against both COX-1 and COX-2 enzymes (IC50s of 3.2 and 2.5 μM, respectively), whereas ibuprofen was approximately 100-fold more potent for COX-2 (IC50 = 0.1 μM) than for COX-1 (IC50 = 11 μM), and indomethacin was about 50-fold more potent for COX-1 (IC50 = 0.012 μM) than for COX-2 (IC50 = 0.56 μM). |
|
| Publications: |
2 |
Organism: |
In Vitro |
| + |
acetylsalicylic acid | down-regulates
chemical inhibition
|
PTGS1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-114377 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11809688 |
Nsaids inhibit cyclooxygenase (cox) isozymes, which are responsible for the committed step in prostaglandin biosynthesis, and this has been considered the primary mechanism by which nsaids exert their antitumorigenic effects. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
oxaprozin | down-regulates activity
chemical inhibition
|
PTGS1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258929 |
|
|
Homo sapiens |
Blood Platelet, Synovial Cell |
| pmid |
sentence |
| 9650852 |
We used human platelets cyclooxygenase-1 and interleukin-1beta-stimulated human synovial cell cyclooxygenase-2 for measuring cyclooxygenase selectivity. The presence of the enzymes was confirmed by immunoblotting and immunoprecipitation analysis, and by the reverse transcriptase-polymerase chain reaction. Mean IC50 values (microM) for human platelet cyclooxygenase-1 and interleukin-1beta-stimulated human synovial cell cyclooxygenase-2 and cyclooxygenase-1/-2 IC50 ratio of various NSAIDs were as follows: aspirin, 3.2, 26, 0.12; diclofenac, 0.037, 0.00097, 38; etodolac, 122, 0.68, 179; ibuprofen, 3.0, 3.5, 0.86; indomethacin, 0.013, 0.044, 0.30; loxoprofen (active metabolite), 0.38, 0.12, 3.2; NS-398, 12, 0.0095, 1263; oxaprozin, 2.2, 36, 0.061; zaltoprofen, 1.3, 0.34, 3.8; respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid | down-regulates activity
chemical inhibition
|
PTGS1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258323 |
|
|
in vitro |
|
| pmid |
sentence |
| 22091869 |
Here we report the application of STD-NMR to characterize the binding of the anti-inflammatory drugs ibuprofen, diclofenac, and ketorolac to COX-1 and COX-2. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
suprofen | down-regulates activity
chemical inhibition
|
PTGS1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257809 |
|
|
Homo sapiens |
PC-3 Cell |
| pmid |
sentence |
| 18667313 |
Profens, that is, Ketoprofen 1, Suprofen 2 (Fig. 1), were chosen because of their interesting inhibitory activity against cyclooxygenase and of their different selectivity versus the two isoforms COX-1/COX-2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTGS1 | up-regulates quantity
chemical modification
|
prostaglandin H2(1-) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269778 |
|
|
in vitro |
|
| pmid |
sentence |
| 7592599 |
[14C]Arachidonate metabolism by oPGHS-1 and hPGHS-2 was examined in reactions with a series of GSP/Cox ratios (Fig. 3). The principal metabolite for both isoforms was the endoperoxide PGH2, with lesser amounts of PGF2a, PGE2, PGD2, |
|
| Publications: |
1 |
Organism: |
In Vitro |
3.0
PTGS1
- 
- 